Mutations in AMBRA1 aggravate β-thalassemia; targeting MYD88 mutations in lymphomas; air pollution and incident VTE risk
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Show Notes
In this week's podcast, a potential new therapeutic target in beta-thalassemia. The E3 ubiquitin ligase AMBRA1 promotes autophagic clearance of free alpha-globin. Researchers describe mutations in the AMBRA1 gene that impair this clearance, exacerbating ineffective erythropoiesis and disease severity. After that: targeting MYD88 mutations. Lasalocid-A is a compound that selectively binds to the MYD88 L265P mutant protein, which is found in a range of B-cell lymphomas. New research shows its potential to inhibit tumor growth, overcome ibrutinib resistance, and synergize with venetoclax. Finally: air pollution is linked to an increased risk of venous thromboembolism in a prospective, community-based cohort study. The findings highlight the harms of pollution, and support the case for global efforts to improve public health.
Featured Articles:
- Mutations in AMBRA1 aggravate β-thalassemia by impairing autophagy-mediated clearance of free α-globin
- Lasalocid A selectively induces the degradation of MYD88 in lymphomas harboring the MYD88 L265P mutation
- Air pollution is associated with increased risk of venous thromboembolism: the Multi-Ethnic Study of Atherosclerosis